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Unknown,Transcriptomics,Genomics,Proteomics

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Deregulated Myc Requires MondoA for Metabolic Reprogramming and Tumorigenesis

ABSTRACT: In order to investigate the effect of MondoA loss on the expression of Myc-dependent genes, we performed a microarray analysis from RNAs isolated from TET21N cells expressing either control (siControl) or MondoA (siMondoA) siRNAs either with (NT) or without (Doxy) induced N-Myc expression. TET21N cells were grown in medium with either Doxy (Myc-Off) or No Treatment (Myc-On), then transiently transfected with either non-specific siRNA or MondoA siRNA in replicates. Cells were then lysed and RNA isolated.

ORGANISM(S): Homo sapiens

SUBMITTER: Lisa McFerrin

PROVIDER: E-GEOD-55538 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Deregulated Myc Requires MondoA for Metabolic Reprogramming and Tumorigenesis

Project description:In order to investigate the effect of MondoA loss on the expression of Myc-dependent genes, we performed a microarray analysis from RNAs isolated from TET21N cells expressing either control (siControl) or MondoA (siMondoA) siRNAs either with (NT) or without (Doxy) induced N-Myc expression.

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Deregulated Myc requires MondoA/Mlx for metabolic reprogramming and tumorigenesis.

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siRIP140 and gene expression effects in E2-treated MCF7 cells

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MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress [ChIP-seq]

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MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress [array]

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Gene expression data from human ovarian cancer cells treated with siRNAs targeting CPNE8 and BHLHE41

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Survival of cells with deregulated MYC requires UVSSA-dependent regulation of RNAPII dynamics

Project description:Cancer cells develop strong genetic dependencies enabling survival under oncogenic stress. MYC is a key oncogene activated across most cancers, and identifying associated synthetic lethality can provide important clues about its activity and potential therapeutic strategies. Based on previously conducted genome-wide screenings we identified UVSSA, a gene involved in transcription-coupled repair whose knockdown decreased cell viability when combined with MYC activation. Synthetic lethal interactions between MYC expression and UVSSA loss correlated with ATM/CHK2 activation, suggesting increased genome instability. We show that although the synthetic lethal interaction was diminished by attenuating RNA polymerase II (RNAPII) activity, it becomes independent of UV-induced damage repair, suggesting that UVSSA has a critical function in regulating transcription in the absence of exogenous DNA damage. Supporting this hypothesis, RNAPII-ChIP-seq revealed that MYC-dependent increase in RNAPII promoter occupancy, as well as RNAPII stalling, is reduced or abrogated by UVSSA knockdown, suggesting that UVSSA negatively regulates MYC-dependent transcription. Taken together, our data shows that the UVSSA complex is required to limit MYC-dependent transcription stress and to maintain cell survival. While the role of UVSSA in regulating RNAPII dynamics has only been documented thus far in the context of UV-induced DNA damage repair, we propose that its activity is also required to cope with transcription stress induced by oncogene activation.

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ERRalpha mediates metabolic adaptations that drive lapatinib resistance in breast cancer (gene expression profiles)

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2016-06-15 | E-GEOD-81546 | biostudies-arrayexpress

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